System for respiratory disorder therapy with stabilization control of stimulation

ABSTRACT

The disclosure relates to a system including a processor configured to generate stimulation control signals in response to a detection of a respiratory disorder. The system further includes at least one kinesthetic effector with a vibrating electromechanical transducer applied to a site on a patient&#39;s skin for delivering a kinesthetic stimulation energy determined by the control signals. The processor is further configured to determine the effectiveness of a stimulation by detecting a cessation of the respiratory disorder. The processor is further configured to extend the stimulation control signals for a determined duration following the cessation of the respiratory disorder.

CROSS-REFERENCE TO RELATED PATENT APPLICATIONS

This application claims the benefit of and priority to French PatentApplication No. 1462041, filed Dec. 8, 2014, which is incorporatedherein by reference in its entirety.

BACKGROUND

The present disclosure relates to the diagnosis and therapy of sleepdisorders.

More particularly, the disclosure relates to a “kinesthetic stimulation”device which is a device for external sensory stimulation of the patientby a vibrator in contact with the skin in a sensitive and precise regionof the body of the patient. Activating this vibrator has the effect oflocally exciting cutaneous or mechanoreceptor endings of the skin, andtriggering a response from the patient's autonomic nervous system, withsympathetic predominance (hereinafter “autonomic response”).

The autonomic response to sympathetic activation is observable on themajor modulator effects of cardiac activity, for example a chronotropiceffect (e.g., a heart rate increase, a decrease in RR intervals, etc.)and an inotropic effect (e.g., heart contractility increase, etc.). Thisautonomic response is also observable on the peripheralvasoconstriction, which is increased during sympathetic autonomicactivation. In addition to these effects on cardiac activity, asympathetic activation causes responses in the respiratory system and/orin the central nervous system (autonomic awakenings).

This is a noninvasive method for acting on a number of sleep disordersin alternative ways to the conventional therapeutic approaches that arebased on the application of a continuous positive airway pressurethrough a face mask (a therapy by CPAP), the use of a mandibularorthosis, and/or electrical stimulation of the hypoglossal nerve, whichinvolves the implantation of a pacemaker.

In particular, the respiratory disease known as “sleep apnea syndrome”(SAS) is characterized by the frequent occurrence (at least 10 to 20times per hour) of apneas during a patient's sleep phase, an “apnea” (orrespiratory pause) being defined as a temporary cessation of breathingfor a duration longer than 10s. SAS can also be characterized by theoccurrence of hypopnea under the same conditions, a “hypopnea” beingdefined as a significant decrease (without interruption) of thebreathing rate, typically a decrease of more than 50% compared to aprevious reference average value.

This pathology reaches more than 4% of the population and more than 50%of patients with heart failure. To protect the individual againstasphyxiation due to the decrease in blood oxygen concentration duringthe interruption or the reduction of respiratory rate, the body adaptsitself but with a deleterious effect on sleep, causing unconsciousmicro-arousals. The consequence is daytime sleepiness when in a wakefulstage, with loss of attention and increased risk of accident.Furthermore, several studies have shown a higher incidence of blooddisorders in patients with SAS such as hypertension, ventriculararrhythmias, myocardial infarction and heart failure.

Several documents describe the ability to stop apnea episodes through astimulation therapy. For example, U.S. Pat. No. 5,555,891 A describes avibrotactile stimulation system to stop apnea in newborns. The objectiveis to provide a system capable of detecting apnea and of stimulating thechild to stop apnea, with a stimulation energy that may vary to avoidhabituation. The applied energy is important and often involves arousal.

WO2007141345 A1 describes a remote monitoring system for neonatal units,to detect and stimulate infant apnea-bradycardia. This applicationrefers to an adjustment of the stimulation energy based on the measuredheart rate of the infant. In the proposed method, no analysis ofrespiratory signals is performed. This prevents the differentiation oftypes of detected or expected sleep disorders, and therefore, theadjustment of stimulation strategies based on said type of disorder.Moreover, this approach limits the delivery of therapy to the timeinterval during which the disorder is present.

WO 96/28093 A1 also teaches a system that delivers a stimulus to reducethe frequency or duration of an apnea episode. At the stimulation level,this document simply describes the low and high limits of thestimulation energy that may stop apnea without waking the patient.

US 2008/009915 A1 discloses a system that detects respiratory disordersusing a nasal or other cannula and applies a particular vibratorystimulation in the ear region. The objective is to stop apnea, withoutwaking the patient, by stimulation which may be manually orautomatically adjusted, depending on physiological characteristics ofthe patient or of the sleep cycles. This document also generally citesthe optimization of the stimulation parameters to fit the severity ofthe patient's disorder, without giving details on the stimulationparameters adjustment. A change in parameters to prevent habituation isalso cited.

US 2010/0048985 A1 describes a similar device for applying stimuli byvarious natures (e.g., audio or ultrasonic stimulation of the ear, eyestimulation, mechanical stirrer, etc.). The device also analyzes therespiratory activity to evaluate the effectiveness of the stimulation sothat the patient or the physician can change the setting of thegenerator as desired with different doses of the stimuli.

US 2008/0154330 A1 describes an electrical stimulation system of thediaphragm to stabilize breathing. Therapy is triggered when arespiratory instability is detected and stopped when a predeterminednumber of stable cycles were detected. No indication is given about apossible optimization of the therapy based on a respiration stabilityanalysis. Moreover, this therapy by stimulation of the diaphragm is notapplicable to obstructive apnea or hypopnea.

Finally, WO 2009/154458 A2 teaches a system which detects apnea and inturn causes an inspiration reflex by stimulation in the ear region.Various apnea detection methods are illustrated. The stimulation may beelectrical or mechanical. The stimulation strategy is minimal; it is toapply pulse trains as long as the disorder is present. However, it isindicated that the stimulation parameters may vary, without, proposedvariation rules. A random variation of the parameters is also cited toavoid habituation. However, this document is very vague on thestimulation parameters. It only very generally discloses:

-   -   Mechanical, electrical or acoustic stimulation;    -   A stimulation frequency between 1 and 500 Hz; and    -   A duration of stimulation and a waiting time between two stimuli        varying between 0.5 and 10 s.

The stimulation will be more or less effective depending on the chosenvalues, for example the brainstem elements have a sensitivity whichvaries greatly with the frequency range. Furthermore, by randomlyvarying the stimulation energy, the risk is a less effective therapy (ifenergy is too low) or waking the patient (if energy is too high).Finally, in this document, the therapy stops as soon as there isrespiratory recovery, such as from the detection of an inspiratoryreflex that is expected to be triggered.

Thus the prior art provides very little teaching on a precise method forthe stimulation delivery. However, a poorly adjusted or randomstimulation can cause:

-   -   Inefficiency, if the stimulation is not appropriate and adapted        to the response that is desired to be caused by the stimulation;    -   Short or medium term addiction resulting in an ineffective        therapy, if the therapy is issued too often or misused;    -   Finally, a patient arousal and therefore sleep disintegration,        which is to be avoided by treating the apnea.

SUMMARY

A first aspect of the present invention relates to a fine adjustment ofstimulation parameters which can have a significant impact on thequality and effectiveness of therapy.

A second aspect of the invention relates to a fine temporal control ofthe stimulation period, especially the stopping time, which can have asignificant impact on the quality and effectiveness of therapy.

More specifically, according to certain aspects, disclosed is a devicefor treating a respiratory disorder in a patient by kinestheticstimulation, including:

-   -   A processor configured to produce kinesthetic stimulation        control signals in response to the detection of a respiratory        disorder; and    -   At least one kinesthetic effector adapted to be applied to a        patient's external skin site, and including a vibrating        electromechanical transducer capable of receiving control        signals and outputting a kinesthetic stimulation energy        determined by the control signals.

According to the aforementioned first aspect, the processor is furtherconfigured to provide automatic determination of the therapy, includingdynamically selecting, based on a type of expected or detected disorder,a strategy of stimulation from a set of stored simulation strategies.

According to various embodiments:

-   -   The stimulation strategies may include at least one strategy by        stimulation pulse of a first type and at least one stimulation        strategy by stimulation pulse of a second type, the pulses of        the second type having a pulse duration greater than the first        type and/or pulses of the second type being spaced apart by a        time interval greater than the pulses of the first type;    -   The pulses of the first type may have a pulse duration between 2        and 3 seconds and are spaced apart by a time interval between 2        and 3 seconds, and the pulses of the second type have a pulse        duration greater than that of the pulses of the first type and        are spaced apart by a time interval greater than the pulses of        the first type;    -   The automatic therapy determination may include capping the        value of the stimulation energy to a maximum value;    -   The automatic therapy determination may include selecting,        depending on the type of expected or detected disorder, either a        high energy stimulation strategy and early therapy, or a low        energy stimulation strategy and later therapy;    -   The automatic therapy determination may include incrementally        raising the energy level from the initial value, as long as an        existing respiratory disorder does not disappear;    -   The automatic therapy determination may include comparing each        incremented energy value to a maximum value;    -   The automatic therapy determination may include forcing the        energy level to a value greater than the maximum permissible        value, upon detection of a severe episode of the respiratory        disorder.

The second aspect cited above utilizes a device including:

-   -   A processor configured to produce kinesthetic stimulation        control signals in response to the detection of a respiratory        disorder; and    -   At least one kinesthetic effector adapted to be applied to a        patient's external skin site, and include a vibrating        electromechanical transducer capable of receiving control        signals and outputting a kinesthetic stimulation energy        determined by said control signals; wherein    -   The processor is further configured to determine the        effectiveness of a stimulation, and is able to detect the        disappearance of the respiratory disorder.

In a manner characteristic of the second aspect, the processor isfurther configured to extend the stimulation control during a determinedstabilization period following the disappearance of the respiratorydisorder.

According to various embodiments:

-   -   Extending the stimulation control may occur after the        disappearance of the disorder pulses with the same duration and        same spacing as those that caused the disappearance of the        disorder;    -   The processor may be further configured to determine the        duration of extension of the stimulation control from a number        of consecutive breathing cycles following the resumption of        breathing at the disappearance of the disorder;    -   The processor may be further configured to monitor the        occurrence of a new episode of respiratory disorder for a given        duration after the end of a disorder episode;    -   The processor may be further configured to change the extension        duration of the stimulation control, depending on whether or not        of a new episode of respiratory disorder during said given        stabilization duration occurs;    -   The processor may be further configured to dynamically adjust        the duration of extension of the stimulation control by a        learning function of possible recurrences observed over time;    -   The processor may be further configured to adapt to limit the        delivery of kinesthetic stimulation energy to a predetermined        number of successively delivered stimulation pulses;    -   The predetermined number of pulses may assume two different        values, depending on the type of respiratory disorder.

BRIEF DESCRIPTION OF THE DRAWINGS

Further features, characteristics and advantages of the presentinvention will become apparent to a person of ordinary skill in the artfrom the following detailed description of preferred embodiments of thepresent invention, made with reference to the drawings annexed, in whichlike reference characters refer to like elements and in which:

FIG. 1 schematically illustrates a system, according to an embodimentthe invention, placed on a patient.

FIGS. 2 and 3 are timing diagrams illustrating stimulation pulsesapplied to a patient, modeling the resulting changes in sympathovagalbalance, respectively, for two different pulse durations.

FIG. 4 schematically illustrates a method of selecting between two setsof stimulation parameters based on the type of observed disorder.

FIG. 5 is a more detailed flow chart of the various steps of theselection and a stimulation application method with different parametersdepending on the type of disorder.

FIG. 6 is a timing diagram illustrating the stopping of the stimulationafter the disappearance of the disorder, according to the prior art.

FIG. 7 is a timing diagram illustrating the stopping of the stimulationafter the disappearance of the disorder, according to one aspect of theinvention.

FIG. 8 is a detailed flowchart of a method of adjusting the stoppingtime of stimulation according to the above aspect.

FIG. 9 illustrates the arrangement of various control functions of thestimulation in a time diagram, according to the teachings of thedisclosure.

DETAILED DESCRIPTION

FIG. 1 schematically illustrates the main components of a system usedfor the implementation of the present disclosure.

The system includes a Holter device 10 connected to various sensors orelectrodes 12, 14, 16, for measuring physiological signals such as heartrate, respiration, oxygen saturation, pulse wave, phonocardiogram, etc.The present disclosure focuses mainly on the respiratory amplitude orrespiratory pressure, which are simple parameters to obtain. Howeverthis measure is not intended to be restrictive and the disclosed systemand methods can be implemented from other physiological signalscollected from the patient as well.

The system further comprises a kinesthetic stimulation device, with agenerator housing 18 producing pulses for control of a stimulationkinesthetic effector 20, consisting, for example, of a vibrator disposedin a sensitive region of the skin, typically (in adults) in the mastoidbone region near the ear. Vibrotactile stimulation applied to the skinby the effector 20 is detected by the sensory receptors ormechanoreceptors of the body, and this information is transmittedthrough sensory nerves to the autonomous central nervous system.

The effector 20 is, for example, a transducer such as C10-100 ofPrecision Microdrives or C2 Tactor of Engineering Acoustics. Thetransducer is of a few grams which can emit vibrations due to anintegrated vibrator excited by pulse trains of variable amplitude andlength, typically at a frequency of 250 Hz which is the nominalresonance frequency of this particular effector, and which is also thefrequency at which the mechanoreceptors of the skin are the mostsensitive. However, other types of effector can be used effectively.

The control box 18 is controlled by a microcontroller and is configuredto adjust the intensity (i.e., the energy) of kinesthetic stimulation bycontrolled variation of the amplitude, the number, the duration, and/orthe frequency of the stimulation pulse trains forming the signal appliedto the effector 20.

The system also includes a housing 22 coupled to the Holter device 10and to the control box 18 by a respective wire or wireless connection24, 26, to receive data from the Holter device 10, process such data,and in response produce information of kinesthetic stimulation controlto be transmitted to the control box 18. Alternatively, data processingand control of the control box 18 can be operated within the Holterdevice 10 and transmitted directly by a link 28 to the housing 18.

Finally, the system is configured to measure the respiratory rate via,for example, a nasal pressure cannula 30 (and/or an oral cannula) orother type of sensor such as a thermistor or a mechanical sensor of theabdomen and/or the thoracic cavity volume changes (e.g., by a beltequipped with sensors sensitive to stretching, etc.). The nasal pressurecannula 30 delivers a ventilatory signal to the Holter device 10 whichis continuously analyzed in order to detect in real time the occurrenceof an apnea or of a hypopnea.

The system operates as follows: when apnea is detected by the Holterdevice 10, the control box 18 triggers a kinesthetic stimulus to triggera response of the autonomic nervous system so that, in response, theautonomic nervous system causes a change in respiration and thereforetriggers a respiratory reflex that stops apnea.

According to exemplary embodiments, the system is able to triggerdifferent stimulation modes, depending on the type of respiratorydisorder.

In this regard, the stimulation mechanism of the events to be treatedhas been adapted in order to optimize the effectiveness of thestimulation. Specifically, hypopneas and apneas are divided into twomain groups: central apnea and obstructive apneas. Thus, although bothtypes of events can generally be stopped by a kinesthetic stimulationusing the system described above, the operating mechanism of thisstimulation should preferably be differentiated to be effective.

First the case of central apnea is described. The operating mechanism ofthe apneas/hypopneas in the system according to the disclosure is basedon stimulation of the autonomic nervous system or sympathovagal reflex.This type of response is easily obtained non-invasively by stimulatingmechanoreceptors in the skin.

Studies show that during sleep, the autonomic nervous system remainsresponsive to external sensory stimuli and causes a physiologicalresponse. Therefore, the application of stimulation on the skin duringsleep triggers a sympathovagal response that acts not only on the heartrate and the blood pressure but also on the breathing characteristics.

Thus the timing diagram of FIG. 2 illustrates an effective stimulationof the sympathovagal balance. Stimulation is performed by pulse bursts(hereinafter “pulses”) during which a mechanical vibration is enabled atthe frequency of 250 Hz, a frequency at which the mechanoreceptors ofthe skin are more sensitive and is therefore optimal for kinestheticstimulation.

The duration of such a pulse corresponds to the achievement of themaximum level of stimulation of the sympathovagal balance. Thus, it isdesirable to trigger reflexes in an effective method dependent on thisstimulation, including increased respiration. In an exemplary method,the duration of the pulses is between about 2 and 3 s.

Once the maximum level is reached, stimulation is stopped to allow thesympathovagal system to recover as quickly as possible. Whensympathovagal balance has returned to its basis minimal level,stimulation can be restarted without loss of efficiency and without therisk of habituation to stimulation. In an exemplary method, the pulseinterval is also between 2 and 3 s.

FIG. 3 illustrates a situation where the stimulation pulses are toolong. The pulses continue while sympathovagal activation has reached aplateau. The extension of the pulses does not increase the efficiency ofstimulation for the reflexes that were maximally engaged at thebeginning of the plateau. In contrast, it slows down the recovery of thesystem that, is saturated. Also, if the first stimulus did not have thedesired effect, the extension of the pulse delays the issuance of thenext pulse, and thus delays the possibility of halting the respiratorydisorder.

Conversely, with too short of stimulation pulses, the risk is noteffectively stimulating the sympathovagal balance and therefore notcausing the expected reflexes (typically an increase in cardiacfrequency, in voltage or in breathing).

In summary, the important parameters of a kinesthetic stimulation forcentral apneas/hypopneas are:

-   -   A mechanical vibration frequency of 250 Hz;    -   A pulse duration of about 2 to 3 seconds; and    -   A pulse interval (recovery time) of about 2 to 3 seconds.

These parameters are used to optimize the sympathovagal response whileavoiding habituation and allowing the therapy to repeat as early aspossible in case of ineffective therapy.

The case of an obstructive apnea/hypopnea is now considered. Theobjective of kinesthetic stimulation in obstructive sleep apnea is tostimulate the nerves of the muscles controlling the breathing, includingthe hypoglossal nerve.

The mechanism explained above may be effective in some episodes or somepeople, since the triggering of the sympathovagal response will alsostimulate nerve functions and therefore the hypoglossal nerve, but thismechanism might not be enough.

It is desirable, unlike with central apnea, to apply a directstimulation of 10 seconds or more to stimulate a maximum number of nervefibers. The frequency of stimulation vibrations preferably remains thesame, around 250 Hz. The purpose is no longer to trigger a reflex but torecruit a maximum number of nerve fibers near the stimulation point.

Between these two therapy possibilities, the selection of the pacingmode is done automatically by the device, in response to differentiationin real time of the central/obstructive episodes, and/or according tothe efficacy of one therapy or the other. FIG. 4 schematicallyillustrates the differentiation and selection between the two respectivestimulation strategies adapted in this example to the two types ofapnea.

Furthermore, the stimulation system of the disclosure is suitable fortreating the clinical events in a differentiated method.

For example, apnea is a serious episode that may lead to rapiddesaturation. Moreover, this disorder, characterized by an absence ofrespiratory flow, is easy to diagnose with good sensitivity andspecificity. Finally, it is important to stimulate an apnea episode asfast as possible because it will be reduced more easily if it is takencare of quickly.

In contrast, a hypopnea is a more common clinical phenomenon, but lesssevere immediately. The detection of hypopnea is more delicate and goodsensitivity is usually accompanied by a poor specificity. This poorspecificity may create a significant number of false positive stimuli,and these over-stimulations can lead to unexpected awakenings.

To address these issues, the system according to the present disclosureis capable of applying a therapy which varies according to the detecteddisorder, preferably in respect to the following aspects:

-   -   Early treatment: apnea will be treated, for example, within 5 to        10 seconds after the detection, in order to act at the earliest;        however, hypopnea will be processed, for example, in a period of        10 to 15 s after detection, which allows the system to avoid        applying a stimulation on false positives or on light and        spontaneously reduced hypopnea;    -   Therapy energy: upon detection of an apnea, one must be sure to        apply an effective, thus potentially higher energy; however, for        a hypopnea, the system can start stimulation with lower energy,        so with less risk of waking the patient, even if this energy        increases if the disorder continues.

While a differentiation between therapies for apnea and hypopnea isproposed in the foregoing, it will be understood that this principle canbe applied to other respiratory disorders, of differentiable respectivetypes. One could, for example, differentiate the therapy depending onthe nature of the apnea (central or obstructive), the nature of hypopnea(central or obstructive), the level of the desaturation accompanying theepisode, etc.

FIG. 5 schematically illustrates the different actions implemented by aprocessing system of the disclosure. In step 500, the system analyzesthe signals provided by the sensors 12, 14, 16, 30 (or only one of them)for performing a differentiation between apnea (block 510) and hypopnea(block 520). If an apnea is detected, the system applies a time delayΔt, for example, 6 s (step 512) prior to determining (step 514) if theapnea is still present. If so, the therapy is applied with the nominalenergy adapted for this type of disorder—a higher energy than for ahypopnea (step 516). If not, the method returns to step 500 of signalmonitoring.

If a hypopnea is detected, the system applies a time delay Δt, forexample 10 s (step 522), and then determines (step 524) if the hypopneaphenomenon is still present. If so, the system determines a minimumlevel of stimulation energy (step 525) and applies a pacing therapy(step 526) with that energy level. Then the system again determines ifthe hypopnea is present (step 527). If so, the level of stimulationenergy is increased by a given increment (step 528) and the therapy(step 526) is implemented with this new energy. Then it is checked againif the hypopnea is present (step 527).

The test of maximum energy (step 529), implemented after each energyincrement, limits the energy level to a ceiling (typically below theenergy level that can cause a patient's waking), and discontinues thetherapy when this energy level is reached. In all cases, the stimulationstrategy itself (including the pulse width and the spacing betweenpulses) is determined by the system dynamically, depending on the typeof disorder (central or obstructive).

A second aspect of the system of the disclosure relates to when thestimulation is stopped after a recovery of respiration.

In the prior art, it is recommended to stop the stimulation when therespiratory signal is present. However, early cessation of stimulationin certain conditions could cause early recurrences of respiratorydisorders, as shown in FIG. 6. FIG. 6 illustrates the case in whichkinesthetic stimulation pulses are applied by the processing moduleafter a specified period At, with appropriate energy. As soon as therespiratory recovery is observed (recovery of the amplitude of thesignal detecting breathing, as illustrated), the therapy stops at therisk, as shown in this example, of an early return of respiratorydisorder.

FIG. 7 shows the system implemented according to the second aspect ofthe disclosure, where the kinesthetic stimulation pulses are extendedbeyond the time where the signal analysis determines the resumption ofthe ventilation. The extension allows the ventilation to sustainablyrecover, while minimizing the risk of early recurrence.

The example illustrated in FIGS. 6 and 7 is that of obstructive apneasor hypopneas.

In some cases, it may also be important to impose a limit on the numberof delivered pulses. Beyond a certain number, it is likely that the lackof response is due to ineffective therapy. Therefore, it may be uselessto continue to deliver pulses unnecessarily, which may awaken thepatient.

The limit may be different depending on the delivered therapy. In thecase of a short pulse therapy which therefore consists of triggering aresponse from the sympathovagal balance, the produced reflex is an“all-or-nothing” type. If the first few delivered pulses (e.g., thefirst three) with appropriate amplitude have failed to trigger thereflex, the therapy is not effective and it is not useful to stimulatemore at the risk of waking the patient. In contrast, in the case oftherapy consisting of long pulses to recruit the nerve fibers, themaximum of number of pulses is greater, typically between 10 and 15pulses, to ensure the maximum of nerve fibers are recruited.

The additional duration, or settling time, which elapses between thedetection of the respiratory recovery and the end of the stimulation maybe fixed or programmable, or dynamically adjusted based on variouscriteria. Thus, learning can be advantageously provided to bestdetermine this duration, expressed for example by the number of breathsto be observed prior to therapy discontinuation and/or depending on anyrecurrence over time.

In the example of FIG. 7, the system applies pulses having the sameduration and the same interval as those that caused cessation of thedisorder after the resumption of respiration. The pulse are applied fora period corresponding to three respiratory cycles of amplitude greaterthan a certain threshold.

FIG. 8 shows the steps implemented by the system to perform thisfunction. Step 800 is the detection of a respiratory disorder. When sucha disorder is detected, a Tx stimulation therapy is selected dependingon the type of disorder (typically apnea/hypopnea, andcentral/obstructive) and applied in step 810.

During therapy application, the system checks in step 820 if the numberof pulses delivered is less than the maximum number allowed for the typeof ongoing therapy, for example three pulses for a short pulse therapy(response of the sympathovagal system) and ten pulses for a long pulsetherapy (recruitment of fibers). If the maximum number of pulses isreached, the therapy is stopped in step 820 even if the ventilatoryrecovery has not taken place, as it is assumed that the therapy is noteffective and should no longer delivering ineffective stimulation, toavoid waking the patient.

Still during application of the Tx therapy, the system detects in step840 if the respiratory activity resumes. If so, steps 850 and 860respectively perform a count of the number of breathing cycles followingthe resumption of breathing (Ctrcycle_stop_Tx parameter) and acomparison of the count with a reference value which indicates thenumber of respiratory cycles, after recovery, for which stimulationshould continue. When the reference value is reached, the system stopsthe application of pulses and resets the value of the Ctrcycle_stop_Txcount (step 870).

Next, at step 880, the respiratory rate is monitored for a period ΔT anda test is performed at step 890 to determine if an apnea or a hypopneaphenomenon occurs during this period. If so, the reference value isincremented by a given value, for example by one unit (step 900), sothat on a subsequent pacing, the stimulation phase after resumption ofbreathing continues for a longer duration.

If not, the reference value is reduced by the same given value, forexample by one unit (step 910), so that on a subsequent pacing, thestimulation phase after resumption of breathing continues for a shorterduration. The reduction of the reference value avoids a systematic driftof the therapy extension duration setting in case of frequentresumptions of a disorder in the post-therapy monitoring.

FIG. 9 illustrates in a time diagram the arrangement and interaction ofthe various features described hereinabove, namely:

-   -   The function of selecting a particular stimulation therapy        adapted to the type of expected or detected respiratory        disorder;    -   The function of dynamically adjusting the energy and temporal        parameters of applied stimulation pulses; and    -   The function of determining a controlled stimulation stop after        the resumption of respiratory activity.

These features are implemented by three specific hardware or softwaremodules respectively M1, M2, and M3 implemented in the housing 22, itbeing noted that the module M2 for adjustment of the stimulationparameters and the module M3 for determination of the stop are active inparallel during the stabilization period.

What is claimed is:
 1. A system for treating a respiratory disorder in apatient by stimulation, including: a processor configured to generatestimulation control signals in response to a detection of a respiratorydisorder; and at least one effector adapted to receive the stimulationcontrol signals and to deliver a stimulation energy determined by thestimulation control signals; wherein the processor is further configuredto determine an effectiveness of the stimulation energy by detecting acessation of a respiratory disorder episode and extend the stimulationcontrol signals during a determined stabilization period following thecessation of the respiratory disorder episode.
 2. The system of claim 1,wherein the extended stimulation control signals are applied after thecessation of the respiratory disorder episode and include pulses with apulse duration and an interval between pulses that are consistent withpulses that caused the cessation of the respiratory disorder episode. 3.The system of claim 1, wherein the processor is further configured todetermine an extension length of the stimulation control signals from anumber of breathing cycles consecutive to the resumption of breathingafter the cessation of the respiratory disorder episode.
 4. The systemof claim 1, wherein the processor is further configured to monitor anoccurrence of a new episode of the respiratory disorder for a givenduration after the cessation of the respiratory disorder episode.
 5. Thesystem of claim 4, wherein the processor is further configured to changean extension length of the stimulation control signals, depending on theoccurrence or an absence of a new episode of the respiratory disorderduring the determined stabilization period.
 6. The system of claim 1,wherein the processor is further configured to dynamically adjust anextension duration of the stimulation control signals by a learningfunction analyzing possible recurrences of an episode of the respiratorydisorder observed over time.
 7. The system of claim 1, wherein theprocessor is further configured to limit the delivery of stimulationenergy to a predetermined number of successively issued stimulationpulses.
 8. The system of claim 7, wherein the predetermined number ofsuccessively issued stimulation pulses can assume two different values,selected by the processor depending on a type of respiratory disorder.9. The system of claim 1, wherein the stimulation is kinestheticstimulation.
 10. The system of claim 9, wherein effector is akinesthetic effector adapted to be applied to a patient's external skinsite, and comprising a vibrating electromechanical transducer.
 11. Asystem for treating a respiratory disorder in a patient by kinestheticstimulation, including: a processor configured to generate kinestheticstimulation control signals in response to detection of a respiratorydisorder; and at least one kinesthetic effector adapted to be applied toa patient's external skin site, and comprising a vibratingelectromechanical transducer adapted to receive control signals and todeliver a kinesthetic stimulation energy determined by said controlsignals; wherein the processor is further configured to determine aneffectiveness of the kinesthetic stimulation energy by detecting acessation of a respiratory disorder episode and extend the stimulationcontrol signals during a determined stabilization period following thecessation of the respiratory disorder episode.